Cas du 30/03/2015: Flow Convergence (PISA Formation) in the LV/LVOT

Presentation: The video shows a flow convergence or PISA formation in the LV/LVOT.

#1: What is the cause of the flow convergence (PISA formation)?
































Explanation: The flow convergence or PISA formation in the LV/LVOT that is sometimes present is due to the flow acceleration of blood out of the ventricle. Since the CFD maximum velocity is 50 cm/sec, any flow that exceeds that velocity will alias, thereby producing a pseudo-flow convergence.   If the LVOT is more perpendicular to the scan line than what is present in this video, the flow may also produce a fake flow convergence or PISA formation. A VSD in the septum with a flow convergence or PISA formation can also be a cause, however, one would expect to see a jet in the RV and, possibly, a defect in the septum. 

Cas du 29/03/2015: A prosthetic mitral valve mass

Presentation: A patient had a MVR (replacement) several years ago and is asymptomatic but had this echo loop.

#1: What is the definition of endocarditis?
#2: What is the diagnosis?
 

Explanation:

The definition of endocarditis requires one of three following requirements being met:

 (Duke Criteria)

1 - Two major criteria are present

2 - One major and three minor criteria are met

3 - Five minor criteria are met

Major Citeria

1. Positive Blood Culture for Infective Endocarditis

2. Evidence of Endocardial Involvement

• oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets,
  or on implanted material in the absence of an alternative anatomic explanation, or
• abscess, or
• new partial dehiscence of prosthetic valve
• new heart murmur

Minor Criteria

1. Predisposition: Predisposing heart condition or intravenous drug use

2. Fever: temperature > 38.0 ° C (100.4 ° F)

3. Vascular Phonomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions

4. Immunologic Criteria: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor

5.Microbiological Evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE
6. Echocardiographic Findings: consistent with IE but do not meet a major criterion as noted above

The patient does not meet the above criteria so this mass is a thrombus.

 

Cas du 28/03/15: A large clot

Presentation: A patient present to the operating room with this loop.

#1: What is the definition of tamponade?

#2: Does this patient have tamponade?

#3: Is the patient compensating for the left atrial compression?

Explanation:

The definition of cardiac tamponade is the accumulation of fluid/blood/effusion in the pericardial sac that causes decreased filling of the heart.

With the left atrial compression, the left atrium is inhibited from filling so tamponade would be present. However, classically, tamponade, when global, also exhibits collapse of the low pressure areas (atria and right ventricle). In localized tamponade, the affected area is located where the clot or tumor is located. In this patient the left atrium is collapsed. One would expect that the right ventricle and right atrium to be enlarged from decreased filling of the left atrium. They are not enlarged. Also, decreased filling of the left ventricle would exhibit a small ventricular cavity. It is not decreased in size. Therefore, this echo indicates that flow is at least getting through the left atrium to minimally fill the left ventricle.

This clot may be pleural in it's location. A small separation of the left atrial wall and the pericardium can be seen in the video which would indicated that the clot is in the pleural space. While pleural clots causing left atrial compression are rare, it would be consistent with what is seen in the RA, RV, and LV.

Cas du 27/03/2015: A Big Jet

Presentation: A patient came to the OR with this echo loop.

#1: What is the type and severity of the valve lesion in this loop?
#2: What is the etiology of the valve lesion?

Explanation: This loop shows severe aortic regurgitation.  The aortic regurgitant jet is > 65% of the LVOT diameter and has a high turbulent pattern. The etiology of the aortic regurgitant jet is an ascending aortic aneurysm.  As the STJ dilates, the AV leaflets are pulled apart and the AR jet is central in all views. The STJ is effaced so the etiology of the ascending aortic aneurysm is probably a connective tissue disorder such as Marfans or Cystic Medial Necrosis,

Cas du 26/03/2015 : Pericardial Effusion

Presentation: A patient came to the OR with this echo loop.  The loop shows a pericardial effusion.

#1: What is the severity of the pericardial effusion?

#2: Please discuss how pericardial effusions are placed into the small, medium, or large category?

Explanation: This effusion is a small pericardial effusion.  Pericardial effusions are classified as small, medium, or large and are < 100ml, 100-500ml, or > 500ml respectively.  Since we can't easily measure the volume by echocardiography, small pericardial effusions are typically behind the inferolateral wall (posteriorly) of the heart.  As the effusion enlarges, it fills up the lateral and apical areas.  A large effusion is global and surrounds the heart.  Typically, large effusions will be global and the epicardial to pericardial distance will be more than 1 cm.

Cas du 25/03/2015: Acute Hypotension

Presentation: A patient was having a total hip knee performed.  Upon the last stitch being placed, the patient suddenly went hypotensive are required epinephrine to resuscitate the patient.

#1: What is your diagnosis?

#2: What therapy would you suggest for this patient?

Explanation: The patient has a massive pulmonary embolism that is occluding the right pulmonary artery.  The view is the midesophageal ascending aorta view with eh right pulmonary artery roofing the ascending aorta.

Two main therapies exist - thrombolytic therapy or surgical therapy.  Surgical therapy is reserved for patients who have a contraindication to thrombolytic therapy or where thrombolytic/anticoagulation therapy is ineffective.  While thrombolytic therapy is perferred, sometimes the patient's hemodynamic status is not conducive to waiting for thrombolytic therapy.  If the patient is somewhat hemodynamically stable, operative embolectomy has a mortality rate around 11%.  If the patient is hemodynamically unstable with moderate/severe right ventricular dilation/dysfunction, hemodynamic collapse, with resuscitation, the mortality rate was 85%.

This patient was hemodynamically unstable and had severe RV dysfunction and required epinephrine infusion to maintain minimal perfusion.  We referred the patient to surgery for emergency embolectomy because of the TKA operation would have lead to excessive bleeding from the thrombolytics.

Cas du 24/03/2015: Post CABG Hypotension

Presentation: A patient developed hypotension post CABG.  This echo loop was obtained.

#1: What is your diagnosis?

#2: Explain the echocardiographic signs that you would expect with this diagnosis?

Explanation: The patient has a pericardial clot causing tamponade.

Signs of tamponade depend upon the pericardial sac and the type of pericardial fluid.  In an intact pericardium, an acute rise in volume can quickly cause tamponade without much volume.  However, in chronic effusions, tamponade may occur with several liters of fluid in the pericardium where the pericardium has had time to enlarge. In the patient with an intact pericardium, the pressure in the pericardium rises and in transmitted to the lower pressure chambers of the heart - the atria.  The atria become collapsed and the preload to the heart is decreased despite high filling pressure to the atria (CVP). As the pressure increases more the right ventricle is the first ventricle to be affected.  If the pressure exceeds the diastolic right ventricular pressure the RV collapses during diastole (diastolic collapse) and eventually, with more increased pericardial pressure the right ventricle fails to fill during systole and diastole.

Post-op CABG patients do not have an intact pericardium. Fluid or blood must collect around the heart to affect the chambers.  Fluid pressure is transmitter throughout the chest, whereas, clots will push on adjacent structure - their pressure is more localized and directed to nearby structures. If a clot is by the left atrium, the left atrium will be affected first.  If the pressure exerted exceeds the atrial filling pressure, the atria become collapsed.  Similarly, the ventricles  become affected.

In this video the clot is pushing on the right atrium and right ventricle, inhibiting the filling of those chambers.  Since the filling is compromised, the ejection is compromised also.  The left atrium and ventricle are hypovolemic and the video shows a small left ventricular cavity that is foreshortened.  A clot also exists around the apex of the heart.

Cas du 23/03/2015: Title: On the LAM

Presentation: A patient presented with a cough and a new murmur.

#1: What is your diagnosis?
#2: Explain the echocardiographic signs of your diagnosis?
#3: Discuss the clinical presentation of this diagnosis?



















Explanation: The loops show a left atrial myxoma (LAM).  LAM are round or oval masses that may be undulating and appear with a ground glass texture.  LAM are mobile and are attached to the left atrium, sometimes by a stalk.  LAM can occur just about anywere in the atrium and TV/MV leaflets.

The clinical presentation is usually a CVA, TIA, palpitations, shortness of breath, dyspnea, ventricular failure, syncope, or chest pain.  The LAM is usually benign but can be cancerous.  Acute hemorrhage into the LAM has ocurred and cause acute occlusion of the MV. Atrial myxomas can be single or multiple, can occur in multiple locations in a single atrium or in both atria.

Cas du 22/03/2015: Right Atrial Sediment

 

Presentation: A patient with atrial fibrillation scheduled for a CABG w/ECC had this loop of his right atrium.

#1: What is your differential diagnosis?
#2: What is the most likely diagnosis?
#3: Could you perform cardioversion on this patient?

















Explanation: The differential diagnosis for a right atrial mass is thrombus, lipoma, artifact, myxoma, vegetation, and tumor.  A linear mass would make it more likely to be a thrombus, lipoma or artifact.  Myxomas, vegetations and tumors do not tend to be linear.  Since the patient is in atrial fibrillation, this most likely represents a thrombus.  Lipomas tend to be more echogenic whereas thrombi tend to be more echo lucent (probably because they are made of blood products sitting in a pool of blood).  Atrifacts or pitfalls would include right atrial pectinate muscles and shadowing from another structure.

Cardioversion is used to convert patients in atrial fibrillation to normal sinus rhythm.  In patients with RA thrombi who are anticoagulated and who do not have a right to left shunt, the risk of stroke or pulmonary embolus is low.  However, patients with RA spontaneous echo contrast and RA thrombi tended to have recurrence of their atrial fibrillation when compared to patients without SEC or RA thrombi.
 

Article sur les masses cavités droites
https://www.dropbox.com/s/j08au879cacf9b5/Echocardiography%20Volume%2027%20issue%209%202010%20%5Bdoi%2010.1111%252Fj.1540-8175.2010.01264.x%5D%20Marina%20Leitman%3B%20Ehud%20Rahanani%3B%20Ilan%20Wassermann%3B%20Simha%20Rosenblatt%20--%20Unusual%20Right-Sided%20Cardiac%20Masses.pdf?dl=0
Et le lien vers les vidéos de l'article:
http://onlinelibrary.wiley.com/doi/10.1111/j.1540-8175.2010.01264.x/suppinfo

Article sur les masses OD:
https://www.dropbox.com/s/edgwtcsz0hyc17x/Echocardiography%20Volume%2022%20issue%205%202005%20%5Bdoi%2010.1111%252Fj.1540-8175.2005.04049.x%5D%20Michael%20S.%20Chen%3B%20Jing-Ping%20Sun%3B%20Craig%20R.%20Asher%20--%20A%20Right%20Atrial%20Mass%20and%20a%20Pseudomass.pdf?dl=0

 Article sur le CS et les thrombi intra-OD dans le cadre du traitement de la FA:
https://www.dropbox.com/s/97ryrfbgkyh3srp/Journal%20of%20the%20American%20Society%20of%20Echocardiography%20Volume%2014%20issue%202%202001%20%5Bdoi%2010.1067%252Fmje.2001.108668%5D%20Bashir%2C%20Mohammad%3B%20Asher%2C%20Craig%20R.%3B%20Garcia%2C%20Mario%20J.%3B%20Abdalla%2C%20Ib%20--%20Right%20Atrial%20Spontaneous%20.pdf?dl=0


Remarque:
Concernant la cardio-version en cas de thrombus OD, dans tous les articles que j'ai lu, les patients ont en bénéficié qu'après disparition des thrombi sous anticuoagulation.

Cas du 21/03/2015: Left Atrial Appendage Velocity

Presentation: We did a PWD of a LA appendage and had a forward velocity of 17 cm/s and a negative velocity of 13-17 cm/sec.

#1: Discuss the normal and abnormal left atrial velocities and their significance?

Explanation: If the velocity of the LAA is low, one would expect that stasis and an environment for thrombus formation would be present. Where you measure LAA velocity is important.  The velocity is higher 1 cm below the LAA orifice than 1 cm from the LAA apex.  The normal LAA velocity exceeds 50 cm/sec.

In patients with atrial fibrillation, the LAA emptying velocity drops.  One study found that elderly patients with low LVEF (< 40%) and a LAA  velocity (LAAV) < 20 cm/sec were more likely to develop LAA thrombi. A TTE will measure about the same velocities as TEE so the modality is not important.  One study showed that TTE measured LAAV at 50 cm/sec were measured at 47 cm/sec.

Cas du 20/03/2015: Left Atrial Appendage

Presentation: A patient  for CABG had this video loop.

#1: What is your differential for this abnormality?
#2: What is the most likely cause of the abnormality?

















Explanation: This video loop shows something near the orifice of the left atrial appendage.  Our differential was thormbus, artifact, or tumor (myoxoma). 
It is very small and the LAA was contracting normally as does the left atrium.  Since there was no stasis, and we felt the shadow was real, we felt that the shadow is myxoma. 
A thrombus can mimick a myxoma and vice versa.
Hemangiomas have occurred in the left atrial appendage but are usually large. While this mass was small, there was no associated signs of stasis, making thrombus less likely.
Although very rare, LAA myxomas have been reported.

Cas du 19/03/2015: RV Abnormality

Presentation: A patient presents for a CABG with some RV abnormalities.

#1: What are the abnormalities of the right ventricle?
#2: Name the differential diagnosis for each of the abnormalities.
#3: Does this patient have diastolic dysfunction causing one of the abnormalities?
#4: What is the most likely cause of the major abnormality?





















Explanation: The abnormalities in this loop is right ventricular enlargement (RVE) and a moderator band.  The moderator band is normal but is sometimes confused with a turmor, thrombus, or artifact.  A moderator band is a pitfall that can be overread and misinterpreted.

The right ventricular enlargement, in this case is more interesting.  The differential diagnosis for right ventricular enlargement fall into three main categories:  increased afterload, increased preload, and decreased contractility.  The RV is not a pressure pump, per se, but can hypertrophy in the presence of longstanding afterload conditions.  Acute increases in afterload will lead to RV dilation and decreased wall motion.  Chronic increased afterload leads to RV hypertrophy and normal wall motion until the afterload is so high that the RV cannot compensate and cause it to dilate and become hypokinetic. High afterload would stent the interventricular septum (IVS) (D shaped IVS) or cause it to bow towards the LV during systole as the RVSP increases.

Increased preload from chronic volume overload (ESRD, TR, PR) or a left to right shunt (ASD) would lead to RV enlargement with normal wall motion until pulmonary hypertension occurred.  Then a mixed pattern would occur.  ASD and TR would cause RAE as would volume overload from ESRD.  The IVS would deviate towards the LV during diastole if the RVEDP exceeded the LVEDP.

In decreased contractility, the wall motion would be decreased from a RV ischemia/infarction. 

A patient with diastolic dysfunction where it affects the right ventricle, causing it to dilate, would first cause left atrial dilation.  Since the left atrium is not dilated, it is very unlikely that diastolic dysfunction is the underlying condition.

In this video, the IVS appears to not deviate during systole or diastole so the RVSP must be higher than normal, otherwise the normal motion for an IVS is to deviate slightly towards the RV.  The wall motion of the RV is normal so contractility is normal and the pulmonary artery pressures are not so high that the RV function is affected.  Since the left side of the heart appears normal - this is probably a process that is right sided only.  Severe PR would cause the TV to close earlier in the diastolic period than the MV which is not the case. We suspect that there is moderate pumonary hypertension from pulmonary causes and other findings will be trivial.

Cas du 18/03/15 : MAPSE

Presentation: A patient had this echo loop.

#1: What is wall motion of the anterolateral wall?

#2: Is there diastolic dysfunction?


















Explanation: The lateral wall cannot be visualized so the wall motion cannot be directly interpreted.  However, indirect interpretation via mitral annular plane systolic excursion (MAPSE) can be predictive of left ventricular ejection fraction.  If the MAPSE is < 12 mm the LVEF is most likely less than 50%.  However, Tissue Doppler appears to be more accurate. MAPSE by M Mode does have correlation with diastolic parameters such as Tissue Doppler peak systolic annular velocity in healthy individuals but there is not effective concordance and cannot be used in place of Tissue Doppler measurements.

In this loop the lateral wall cannot be interpreted, but, given that the septal wall is hypokinetic, the apex is akinetic and the MAPSE appears less than 12 mm, we could estimate that the ejection fraction is less than 50% and the lateral wall is most likely not normal.  MAPSE does not indicate the diastolic dysfunction of the left ventricle.

Further reading:

http://ehjcimaging.oxfordjournals.org/content/7/3/187.long

Mitral annular motion as a surrogate for left ventricular function: Correlation with brain natriuretic peptide levels

Results MAPSE < 12 mm determined by MME has 90% sensitivity, 88% specificity & 89% accuracy for detection of LVEF <50%, while these values were 94%, 93% & 94% respectively for (Sm) < 8 cm/s determined by PWDTI. BNP level >75 pg/ml has 98% sensitivity, 90% specificity & 97% accuracy for detection of LV Dys either (S,D, or both). BNP levels were significantly higher in patients with combined (S & D) Dys. Than those with only (S) Dys, the later group had significantly higher BNP levels than those with only (D) Dys. (1054.5 ± 202.3 pg/ml vs. 500 ± 39.9 pg/ml & 500 ± 39.9 pg/ml vs. 215.3 ± 100.9 pg/ml respectively, P < 0.001) & each were significantly higher than control group (12.3 ± 5.7 pg/ml, P < 0.001). Significant correlations (P < 0.001 for all) were found between BNP levels and Em (r =−0.82), Sm (r=−0.7), early transmitral (E) to Em ratio (r=0.61), MAPSE (r=−0.54), LVEF(r=−0.64) & LV end D dimension (r=0.63).

Conclusion MME and PWDTI used for assessment of MAM are useful methods for evaluation of LV function but parameters measured by PWDTI correlate more strongly with plasma BNP levels than those measured by MME and provide a simple, sensitive, accurate and reproducible tool for early diagnosis of LV dysfunction.

http://www.cardiovascularultrasound.com/content/11/1/16#B12

Mitral annular plane systolic excursion (MAPSE) in shock: a valuable echocardiographic parameter in intensive care patients

Compared to survivors, non-survivors had a significantly lower MAPSE (8 [IQR 7.5-11] versus 11 [IQR 8.9-13] mm; p= 0.028). Other univariate predictors were age (p=0.033), hsTNT (p=0.014) and Sequential Organ Failure Assessment (SOFA) scores (p=0.007). By multivariate analysis MAPSE (OR 0.6 (95% CI 0.5- 0.9), p= 0.015) and SOFA score (OR 1.6 (95% CI 1.1- 2.3), p= 0.018) were identified as independent predictors of mortality. Daily measurements showed that MAPSE, as sole echocardiographic marker, was significantly lower in most days in non-survivors (p<0.05 at day 1–2, 4–6).

Conclusions

MAPSE seemed to reflect LV systolic and diastolic function as well as myocardial injury in critically ill patients with shock. The combination of MAPSE and SOFA added to the predictive value for 28-day mortality. 

http://ehjcimaging.oxfordjournals.org/content/14/3/205

Clinical implication of mitral annular plane systolic excursion for patients with cardiovascular disease

MAPSE and ejection fraction

The average normal value of MAPSE derived from previous studies for the four annular regions (septal, anterior, lateral, and posterior) ranged between 12 and 15 mm^3,14 and a value of MAPSE <8 mm was associated with a depressed LV EF (<50%) with a specificity of 82% and a sensitivity of 98%.³ 

A mean value for MAPSE of ≥10 mm was linked with preserved EF (≥55%) with a sensitivity of 90–92% and a specificity of 87%.^16,19 In addition, a mean value for MAPSE of <7 mm could be used to detect an EF <30% with a sensitivity of 92% and a specificity of 67% in dilated cardiomyopathy patients with severe congestive heart failure.¹⁴ 

It is of note that the association between MAPSE and EF is only valid in case of normal or dilated left ventricles,^20,21 while the correlation is rather poor in patients with LV hypertrophy.

Hypertensive heart disease

The impairment in the contractile function of LV longitudinal fibres may substantially precede that of LV circumferential fibres in patients with hypertension because of LV hypertrophy, geometry, and wall stress.⁵ This might explain the ‘early’ reduced longitudinal function (= MAPSE) in contrast to the long time preserved circumferential and radial function (= EF). Thus, reduced MAPSE can be used as a sensitive early marker of LV systolic dysfunction in hypertensive patients.⁴⁸
 

Coronary artery disease

Willenheimer et al.⁵⁵ demonstrated that MAPSE was reduced in 88 out of 1350 consecutive patients with visual evaluated normal LV regional wall motion and these patients with reduced MAPSE had either prior myocardial infarction (60%) or coronary artery disease without infarction (33%), or uncontrolled hypertension (2%) while definitive evidence for cardiovascular diseases was absent in only 4% patients with reduced MAPSE. This suggests that decreased MAPSE, in the case of normal LV regional wall motion, could serve as a echocardiographic functional sign for myocardial abnormalities, predominantly indicating subendocardial dysfunction.⁵⁵

Aortic stenosis

^{MAPSE could be used as a predictor of long-term prognosis for patients receiving aortic valve replacement operation and MAPSE >7 mm is linked with satisfactory functional improvement after aortic valve replacement. 
In the clinical setting, it is sometimes difficult to distinguish between moderate AS with low gradient and severe AS with low gradient due to reduced stroke volume. A recent study found that MAPSE was useful to distinguish between these two entities.57 In patients with an isolated low-gradient AS, a cut-off value of MAPSE <9 mm had an excellent sensitivity (100%) and specificity (100%) to distinguish between moderate and severe AS .}

Implication for prognosis and therapy

MAPSE is of prognostic importance in the risk stratification for patients with atrial fibrillation,⁶¹ patients post-myocardial infarction,⁶² and patients with heart failure.^15,63,64 Cardiac mortality was 44% in atrial fibrillation patients with an MAPSE <7 mm during 45 months follow-up.⁶¹ In post-myocardial infarction patients with MAPSE <8 mm, the combined mortality/hospitalization incidence was 43.8%.⁶² Sveälv et al.⁶⁴ showed that 10 years survival was significantly better in heart failure patients with highest MAPSE (>9 mm) than in heart failure patients with the lowest MAPSE (<5 mm) (Figure 5). Interestingly, significant correlation was found between serum BNP levels and MAPSE (r = −0.54, P < 0.001).³¹

Limitation of MAPSE

Some of the variations of MAPSE are due to cardiac size. Theoretically, this means that the annular displacement should be normalized for heart size. This is definitely necessary in children, where the variation in cardiac size is great. 

The interpretation of MAPSE should be carefully applied in case of a mobile apex, such as large pericardial effusion. Also in patients with paradox septal motion, because of severe right heart dysfunction, septal MAPSE is not only reflecting LV function but rather RV abnormalities. Thus in these patients, the lateral MAPSE should be used. It is to be mentioned that MAPSE, as opposed to global longitudinal systolic strain assessment, cannot detect regional areas of dysfunction.

After cardiac surgery, septal MAPSE, together with RV function, might be more reduced compared with lateral MAPSE.

Sometimes in patients with mitral valve disease, the mitral ring is extremely calcified. In these patients, the direct MAPSE measurement at the mitral ring is not possible and longitudinal functional assessment should be done slightly more above in the myocardium.

Another limitation of this parameter is that small localized abnormalities (i.e. small areas of fibrosis) cannot be detected as it is only possible to assess longitudinal function of the complete wall.

 

 

 

Cas du 17/03/2015

Presentation: A patient had this LV M Mode scan.

#1: What is this patients ejection fraction (estimate please)?


#2: Is it accurate?

Explanation: This scan is a M Mode scan of the left ventricle short axis.  The endocardial walls are easily visible so the ejection fraction (> 50% in this case) is easily calculated.  

The ejection fraction from a M Mode scan of the LV SAX view is very accurate in most cases except where remote wall motion abnormalities are present.  

However, even in the presence of remote wall motion abnormalities, this calculation is fairly accurate because all of the coronary arteries supplied myocardium are present in this view and significant remote wall motion is unlikely.  

About the only serious wall motion abnormality that would make this scan inaccurate would be a distal LAD lesion where the whole apex is akinetic or dyskinetic thereby decreasing the ejection fraction signficantly.

Cas du 11/03/2015 : Dyskinésie septale

Présentation:
Enregistrement de la coupe ETO suivante chez un patient.

Questions:
Décrivez la cinétique.
Quels sont les étiologies possibles à cette anomalie de la cinétique ?





















Réponses:
La vidéo montre un dyskinésie septale, par ailleurs, la contraction reste bonne.

Les causes possibles sont la stimulation VD, le bloc de branche droit complet, le bloc de branche gauche complet, et certains troubles non spécifiques de la conduction.

Dans la stimulation VD et le BBGc, la contraction du septum inter-ventriculaire se fait en premier, avant la contraction du reste des parois, la dyskinésie se voit en télé-systole, lorsque le reste du VG se contracte alors que le septum entame sa relaxation.

Dans le BBDc, le VG se contracte contre le septum inter-ventriculaire créant une  dyskinésie septale en proto-systole, puis le septum se contracte.

En cas de troubles non-spécifique de la conduction, la dyskinésie est soit proto-systolique ou télé-systolique selon l'atteinte anatomique.


Dans cette vidéo, la dyskinésie septale se fait en proto-systole, ce qui est en faveur d'un BBDc.


N.B: Dans l'article original, l'auteur parle aussi de l'insuffisance mitrale sévère comme étiologie possible de la dyskinésie par l'afflux  brusque du sang, créant une dyskinésie en pré-systole. Je ne l'ai pas rajouté parce-que je ne suis pas d'accord.

Cas 10/03/2015

Présentation:
L'image échographique suivante montre des colonnes charnues  au niveau de l'atrium gauche.

Questions:
#1: Quels sont les caractéristiques des muscles pectinés de l'auricule gauche?

#2: Quels sont les caractéristiques du thrombus de l'auricule gauche?

#3: Quel est votre diagnostic ?

























Réponses:
Les muscles pectinés de l'auricule gauche se présente à l'échocardiographie sous  forme de colonnes, typiquement multiples et parallèles, souvent orienté selon le petit axe de l'auricule.
A l'état normal, l'auricule gauche n'est pas dilatée et il n'y a pas de contraste spontanée eau niveau de l'oreillette gauche (OG). Il n'y a pas de signes en faveur d'un ralentissement du flux sanguin atrial (rétrécissement mitral, dysfonction VG, dilatation ou dysfonction atrial).

Le thrombus de l'auricule gauche est souvent associée à un ralentissement du flux sanguin atrial. L'auricule gauche est souvent dilatée, et l'OG présente un contraste spontané. Une FA est fréquente.
Le thrombus se localise au fond de l'auricule et croît en direction de son abouchement jusqu'à ce qu'il rencontre une zone de haute vélocité où le thrombus ne peut se former, c'est-à-dire l'abouchement de l'auricule gauche ou un peu plus en distalité. Le thrombus apparaît généralement homogène et peut être fixe.

La vidéo montre un auricule normal avec ses muscles pectinés.